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Abstract: “Gluten sensitivity” has become commonplace among the public. Wheat allergy (WA) and celiac disease (CD) are well‐defined entities, but are becoming a fraction of individuals following a gluten‐free diet (GFD). Wheat allergy has a prevalence of <0.5%. Wheat, specifically its omega‐5 gliadin fraction, is the most common allergen implicated in food‐dependent, exercise‐induced anaphylaxis. CD is a non‐IgE hypersensitivity to certain cereal proteins: gluten in wheat, secalin in rye, hordein in barley, and to a lesser extent avenin in oat. It is a rare disease, with an estimated prevalence that varied widely geographically, being higher in Northern Europe and the African Saharawi region than in South‐East Asia. In addition to suggestive symptoms, serologic testing has high diagnostic reliability and biopsy is a confirmatory procedure. Patients with CD have extra‐intestinal autoimmune comorbid conditions more frequently than expected. A third entity is nonceliac gluten sensitivity, which has been created because of the increasing number of subjects who claim a better quality of life or improvement of their variety of symptoms on switching to a GFD. The phenomenon is being fueled by the media and exploited by the industry. The lack of a specific objective test has been raising substantial controversy about this entity. Allergists and gastroenterologists need to pay attention to the multitudes of individuals who elect to follow a GFD. Many such subjects might have WA, CD, or another illness. Providing them with appropriate evaluation and specific management would be of great advantages, medically and economically. [ABSTRACT FROM AUTHOR]

Serum IgD levels in 83 healthy adults were measured by a radioimmunoassay technique and analysed according to each subject's smoking habit. The IgD geometric mean in cigarette smokers was twice as high as in non-smokers (408.6 vs 202.0 μg/dl). Serum IgD levels of 1,000 μg/dl or greater were noted in 22% of smokers but in none of the rare smokers or non-smokers. In the smokers group, the highest mean IgD level was found in those who did not actively inhale the smoke (7626 μg/dl), followed by that in moderate smokers (5638 μg/dl), and was lowest in heavy smokers who inhaled the smoke (2830 μg/dl). The number of years a person smoked did not appear to have a significant effect on IgD levels. In exsmokers, the mean IgD level (199.8 μg/dl) was similar to that in non-smokers, suggesting reversibility of the IgD changes following cessation of smoking. It seems prudent that the smoking habit should be taken into consideration in the interpretation of serum IgD levels. [ABSTRACT FROM AUTHOR]

. Information derived from the compulsory national scheme of medical registration of births in Norway has been utilized in a study of the course and outcome of pregnancy in women with epilepsy. The series comprises 371 pregnancies in women with epilepsy and, as controls, 112530 pregnancies in women reporting no disease before or during the pregnancy. Comparisons indicate that women with epilepsy experience an excess of complications during pregnancy and labour, and that their babies are more frequently born prematurely and of low birth weight, and moreover have an excess of congenital malformations and higher perinatal and neonatal mortality rates. Epileptics, undoubtedly, constitute a high risk group in need of special attention during pregnancy and special care during labour. A proper interpretation of the findings in terms of causation, however, will call for additional data obtainable only through especially designed inquiries. [ABSTRACT FROM AUTHOR]

Discusses sex differences in urinary tract infections in children. Earlier onset, a shorter delay in diagnosis, and a shorter duration in boys; Higher frequency of malformations, a greater number of rehospitalizations, and a greater need for surgical intervention in boys; Proteus infection; Enterococcus and Staphylococcus were more frequent in girls.

Summary: We describe the case of a 24-year-old male with hyper-IgE syndrome (HIES) which was diagnosed at 4 years of age and died from a very rare cardiac complication. He had typical clinical and laboratory manifestations of HIES, including total serum IgE as high as > 100,000 IU/mL. Stem cell transplantation was not available. During the 20-year follow-up, he suffered numerous various infections of the skin and deep organs, partial lung resection, as well as multiple bone fractures. At age 24, he developed acute decompensated heart failure associated with elevated serum troponin I and brain natriuretic protein. Two-dimensional echocardiogram revealed global hypokinesis of the left ventricle with estimated ejection fraction 20-25%, and catheterization revealed ectasia of multiple coronary arteries. Endomyocardial biopsy showed lymphocytic myocarditis, focal necrosis, mild fibrosis, and myxoid degeneration, but cultures were negative. The patient improved on corticosteroid therapy and was discharged on heart failure therapy and external defibrillator. Six weeks later, he developed supraventricular tachycardia and persistent global hypokinesis and was treated with amiodarone. A trial of intravenous immunoglobulin was initiated and was repeated as outpatient every four weeks for four times. However, his cardiac function did not improve and he developed severe hypotension and pulseless electrical activity arrest. Resuscitation was unsuccessful. To the best of our knowledge, this is the first reported case of HIES complicated with lymphocytic myocarditis. Both immunologists and cardiologists need to be aware of such a complication and practice caution in using immunosuppressants when the patient's immune status is markedly compromised.

Background: Food allergy has been gaining increasing attention, mostly as causing gastrointestinal and cutaneous reactions. Its role in asthma seems to be under-recognised., Objectives: This study's aim is to explore the frequency of involvement of a common food, namely cow's milk, in childhood asthma., Methods: 32 children (5 months to 11 years; median 24 months; mean 34 months) with asthma and a suspected history of cow's milk allergy were studied. They underwent skin prick testing (SPT) and specific IgE (sIgE) testing to whole cow's milk (WCM), casein, α-lactalbumin, and β-lactoglobulin, followed by single-blind oral milk challenge., Results: Reactions to milk challenge occurred in 12 (37.5%) including wheezing in 5 (41.7%, or 15.6% of the whole group). Children who developed wheezing at the time of challenge were younger than those who had negative challenge (23.0 months vs. 34.8 months). Challenge was positive in 33.3% of subjects who had a positive SPT, and SPT was positive in 50% of challenge-positive subjects. Regarding sIgE, challenge was positive in 26.7% of sIgE-positive subjects, and sIgE was positive in 33.3% of challenge positive subjects. Skin or serum testing with individual protein fractions did not seem to add significant advantage over testing with WCM alone., Conclusion: This study shows that cow's milk can cause wheezing in children with asthma. Although SPT seemed to be more reliable than sIgE testing, both had suboptimal reliability. It is worth considering possible milk allergy in children with asthma, particularly when poorly controlled in spite of proper routine management., (Copyright © 2012 SEICAP. Published by Elsevier Espana. All rights reserved.)

Background: Studies on serum IgE levels during pregnancy are limited., Objective: To investigate the course of serum total IgE levels during pregnancy and postpartum., Methods: 159 pregnant subjects provided 218 serum samples during various stages of pregnancy and the postpartum period. Serum total IgE geometric means were compared at various trimesters and postpartum. In addition, the postpartum IgE data were analysed according to the method of delivery. Analysis was also done according to history of allergy., Results: The geometric mean serum total IgE was 20.5 IU/ml in the first trimester, 20.8 IU/ml in the second and 22.2 IU/ml in the third. Postpartum serum IgE level showed a lower mean, 14.9 IU/ml during the early postpartum period (less than 30 days) compared to 30.3 IU/ml during the late postpartum period (30 days-25 weeks). However this was not statistically significant. Serum IgE in the postpartum period also did not differ according to method of delivery. A history of allergy was positive in 98 samples, negative in 61 and unclear in 59. Using analysis of variance, none of these three groups showed significant change in serum total IgE level during pregnancy or postpartum., Conclusion: In this cross-sectional study, serum total IgE levels showed no statistically significant changes during pregnancy or postpartum. This finding would be of greater weight if reproduced in a larger number of subjects with multiple serial samples at fixed regular time intervals during pregnancy and postpartum., (Copyright © 2010 SEICAP. Published by Elsevier Espana. All rights reserved.)

Background: The role of genetics in allergy development is well accepted. However, studies could not delineate the mode of inheritance or what is specifically being inherited. The purpose of this study was to determine the effect of genetics on the development of allergy manifestation, serum IgE level, and sensitization to specific allergens., Methods: Fifty-eight twin sets (age 7 months to 11 years) were evaluated for allergy by medical history, family history, physical examination, serum total IgE level, and percutaneous testing to selected common allergens., Results: In 25 monozygotic (MZ) sets, concordance of atopy was significantly higher than in 33 dizygotic (DZ) sets (84.6% vs 62.5%). The age at onset tended to be earlier when the mother was allergic than when the father was (23.5 months vs 30.5 months). When both twins were allergic, the intra-pair difference in age at onset was within <6 months in 50% of MZ sets versus 31.8% in DZ sets. Total IgE level in twins showed a very strong correlation in MZ sets (r 0.92), but only a moderate correlation among DZ sets (r 0.57). Skin test positivity to specific allergens did not show a significant concordance between twins in either group., Conclusion: Our study indicates that the genetic influence was strongest on the inheritance of IgE phenotype, the development of the atopic tendency, the age of onset, and to some extent on the specific allergy manifestation. The effect seemed less on determining the specific offending allergen(s), suggesting possible roles of epigenetic and environmental factors., (Copyright 2009 SEICAP. Published by Elsevier Espana. All rights reserved.)

Objective: This review is intended to provide an outline for the evaluation of patients suspected of having immunodeficiency, a problem that is frequently encountered in clinical practice., Data Sources: Information was obtained through a MEDLINE literature search as well as from standard textbooks in immunology. Also included is information that reflects the authors' clinical experience in the field., Results: In general clinical practice, many physicians feel inadequate to evaluate patients with suspected immune deficiencies. They also think that the process of evaluation is time-consuming, which results in misdiagnosis of a substantial percentage of such disorders. Hence, the prevalence of immunodeficiency disorders is much higher than generally thought. At present, there are >80 unique primary immunodeficiency conditions and >50 syndromes that are associated with various immunologic defects. The prevalence of secondary immunodeficiency has also been increasing because of the tragic epidemic of HIV infection, more usage of immunosuppressive medications and bone marrow stem cell transplantation, and the severe degree of malnutrition in underdeveloped countries. It is necessary for clinicians, particularly the specialists in allergy and immunology, to be able to evaluate the status of the immune system., Conclusions: Very valuable information can be gathered from the medical history and physical examination that may exclude or increase the suspicion of immunologic defect. Laboratory tests can then be appropriately selected to define the specific defect. Once the diagnosis has been settled, proper medical management can be instituted with subsequent improvement in morbidity and mortality of such disorders.

Background: Ingestion is the principal route for food allergens, yet some highly sensitive patients may develop severe symptoms upon skin contact., Case Report: We describe five cases of severe food allergic reactions through skin contact, including inhalation in one., Methods: The cases were referred to a university allergy clinic, and evaluation comprised detailed medical history, physical examination, skin testing, serum total and specific IgE, and selected challenges., Results: These cases were found to have a strong family history of allergy, early age of onset, very high total serum IgE level, and strong reactivity to foods by skin prick testing or RAST. Interestingly, reactions occurred while all five children were being breast-fed (exclusively in four and mixed in one)., Conclusions: Severe food allergic reactions can occur from exposure to minute quantities of allergen by skin contact or inhalation. Food allergy by a noningestant route should be considered in patients with the above characteristics.

Objective: This presentation is designed to critically review information on presentations of food hypersensitivity reactions that may be considered unusual regarding the source or nature of allergen, route of exposure, or clinical manifestation., Data Sources: Information has been gathered primarily through a thorough search of the English literature relevant to human subjects. Some clinical cases were also included from the author's own clinical experience., Study Selection: Information summarized here was critically selected on the basis of proven or acceptable scientific validity., Results: The findings indicate that food allergy presentation can be unusual in three main aspects. First, the offending allergen may not be the obvious food that was ingested or be a food protein incorporated in a nonfood product. Second, systemic reactions can be provoked by very minute quantities of food allergens that may even get access through noningestant routes, eg, inhalation, odor, skin contact, or mucous membrane contact. Third, the clinical manifestations are not limited to the few gastrointestinal, cutaneous, and respiratory symptoms with which we are generally familiar., Conclusions: The extent of food allergy presentation is more than has been generally realized. Our awareness of such unusual presentations adds new knowledge and should prompt our interest in carefully evaluating patients with obscure allergic reactions for possible food allergy.

Objective: This review is intended to be an authoritative summary of the pathogenesis of osteoporosis, a problem that may be encountered in allergy practice. It also provides an outline for identification of subjects at high risk and directions for their appropriate evaluation, management, and prevention of the disease., Data Sources: References were obtained through a MEDLINE literature search as well as from previous reviews. Relevant articles were critically reviewed and their conclusions were included., Results: Osteoporosis is a relatively common disease that is associated with significant morbidity and mortality. The management and prevention of osteoporosis have been improved by an increased awareness of the magnitude of the problem, a better understanding of the pathogenesis, development of a better technique for assessment of bone mineral density, and the availability of specific medications. With the increase in human life-span and the increasing use of glucocorticosteroids for a wide variety of diseases, the incidence of osteoporosis has been on the rise., Conclusion: Glucocorticosteroids are the most common medications that cause or contribute to the pathogenesis of osteoporosis and have been widely used in allergy practice. It is important for physicians to appreciate the current basic understanding of osteoporosis and to be able to identify patients at high risk for this serious disorder, and to initiate appropriate intervention at a sufficiently early time to be effective. Medications for treatment and prevention of osteoporosis include: calcium, vitamin D, estrogen, bisphosphonates, calcitonin, and others are reviewed in this article.

Objective: Pancreatic enzyme is essential in the treatment of cystic fibrosis (CF), but intolerance to it occasionally occurs. We encountered a child who was intolerant to multiple commercially available preparations of pancreatic enzymes and, hence, desensitization was attempted, with success., Case Presentation: A 33-month-old girl was diagnosed with CF at 6 months of age. Initially, she was started on Pancrease MT 16, which was subsequently discontinued because fecal fat studies were normal and she seemed to do well on Nutramigen and vitamin supplements. At 29 months of age, she developed diarrhea with bulky stools and weight loss. A fecal fat 72-hour study revealed a coefficient of absorption of 50%. She was treated with Pancrease MT 16, but had consistent vomiting 1 to 2 hours after administration of enzymes. The vomiting occurred on switching to different pancreatic enzymes preparations, ie, Creon 10, Viokase, and Pancrease MT 16. Vomiting occurred even with small doses of enzymes disguised in food. She had no history suggestive of gastroesophageal reflux, peptic ulcer, or pork allergy, and no vomiting on days when enzymes were not given. This was suggestive of type I hypersensitivity reaction. Pancreatic enzymes were discontinued, and she was given a low-fat, high-carbohydrate diet with satisfactory weight gain., Methods: Double-blind, placebo-controlled titrated oral challenges with pancreatic enzymes resulted in definite vomiting within 1 to 1.5 hours after challenges with Viokase and Pancrease MT 16, but not with placebo. Rush oral desensitization with Viokase solution was attempted, starting with 5 mg, and the dose was doubled every 20 minutes, aiming to reach a cumulative dose of 700 mg. However, the child vomited when a cumulative dose of 315 mg was reached. Another trial of slower desensitization was done using Pancrease MT 16 (1 capsule: 16 000 U of lipase, 48 000 U of amylase, and 48 000 U of protease), starting with 1/4 capsule per day, with increments of 1/4 capsule every 3 days, until an entire capsule was reached by day 10, then increased by approximately 1/2 capsule every 4 days until reaching the therapeutic dose of 1 capsule with each meal by day 25., Results: The patient tolerated this fairly well and has been on this treatment and regular diet for >1 year, without any adverse reaction. This illustrates a rare case of gastrointestinal adverse reaction to pancreatic enzymes that was treated successfully with desensitization., Conclusion: Pancreatic enzyme intolerance, although rare, would be a major problem in the management of patients with CF. Hence, desensitization would be essential and may be accomplished successfully using the protocol described in this report.

Because food allergy treatment is basically avoidance of the offending food(s), identification of the latter becomes the cornerstone for management. At present, the elimination-challenge test is the most definitive procedure for verification of a cause-and-effect relationship between a particular food and a certain reaction, allergic or not. The oral challenge test is most reliable when conducted in a double-blind, placebo-controlled manner. In routine clinical practice, however, single-blind testing is satisfactory in most cases. Open challenge testing might be acceptable in young children or for screening the least suspected foods. It would be prudent to avoid the test, in any of its forms, in instances where a specific food caused a life-threatening reaction. Caution needs to be practiced in planning, conducting, and interpreting the results of challenge tests. Difficulties may be encountered in disguising the test food, choosing a placebo, reproducing the natural exposure, incorporation of possible associated factors, and avoiding any bias on the patient's or observer's part.

For an infant to develop allergy (atopy), three main factors seem to be needed: genetic predisposition, allergen exposure, and contributory factors. The role of genetics seems to be mainly in transmitting a general atopic constitution and controlling the general IgE response. Together with environmental exposure, genetics possibly plays a role in determining the allergic shock organ and the specific offending allergen. Of the vast number of environmental allergens, food by far seems to be the major one in infancy, followed by indoor allergens then outdoor aeroallergens. Several intrinsic and extrinsic contributory factors can enhance the development of allergy, perpetuate its chronicity, or facilitate precipitation of symptoms. These factors can be immunologic defects, gastrointestinal diseases, infections, or nonspecific irritants such as tobacco smoke inhalation. Understanding all these factors is essential in formulating any program for allergy prevention in infants.

The role of food allergy in the respiratory tract is often underestimated. A wide variety of food-induced respiratory symptoms has been described. In some patients, a food additive rather than a food protein is the offending agent. This presentation focuses on food-induced asthma and milk-induced chronic pulmonary disease in infants.

In clinical practice at present, milk allergy may be suspected by medical history, skin testing, or RAST. None of these procedures has shown an optimal correlation with the result of challenge testing. The obvious need for better diagnostic tests has stimulated numerous attempts to improve the current tests and to develop new ones. The use of individual milk protein fractions for skin testing or RAST has not shown superiority over using whole cow's milk. Lymphoblast transformation and leukocyte inhibition factor production have shown low specificity. The few studies on neutrophil chemotactic activity have shown contradictory results. Morphometric and immunohistochemical studies of small intestinal biopsy specimens seem to be more suitable for research studies than for routine clinical practice. The reliability of in vitro tests on cultured intestinal epithelium remains to be verified and is far from being applicable in clinical practice. The diversity of immunologic mechanisms of milk allergy is largely responsible for the difficulty encountered in developing a highly reliable test in the diagnosis of various reactions to milk allergy.

Food allergy is one of several causes of adverse reactions to foods. The underlying immunologic mechanism varies from one manifestation to another, hence no current single laboratory test can be expected to be positive in every case. The diagnosis could be suggested by information gathered from the medical history or screening procedures, such as trials of elimination diets, the food/symptom diary, skin testing, and in vitro-specific IgE antibody measurement. All foods suspected by any of the aforementioned methods should be subjected to verification by appropriate elimination-challenge testing, preferably in a double-blind, placebo-controlled manner. Basically, treatment is dietary elimination, and its success requires identification and avoidance of all offending foods and control of other contributory factors.

The atopic status of patients with leprosy was assessed by medical history, physical examination, serum total IgE, and specific IgE antibodies to common allergens (by skin testing and RAST). Tests for specific IgE antibody to Mycobacterium leprae were performed by RAST and immunoblotting technique. We studied 28 patients with leprosy and 49 control subjects. The two groups did not differ significantly in the prevalence of atopic disease. The IgE level was significantly higher in the patients, however, than in the control subjects, whether there was atopy (296.1 versus 96.3 IU/ml) or not atopy (72.9 versus 18.9 IU/ml). Neither RAST nor immunoblotting technique detected significant levels of IgE antibodies to M. leprae. Our data indicate that leprosy was associated with increased total IgE level, but clinical atopy in patients with leprosy was similar to that in control subjects. The observed IgE increase in patients with leprosy appears to be generally nonspecific.

Serum IgE levels in healthy blood donors who had no history of atopy were measured by a paper-disc RIA and analyzed according to the donors' smoking habits. The IgE geometric mean for regular smokers was 41.7 IU/ml, which was significantly higher than that for nonsmokers (19.3 IU/ml) or rare smokers (22.7 IU/ml). Whereas 28% of smokers had IgE levels greater than 200 IU/ml, none of the rare smokers or nonsmokers did. IgE levels in smokers showed a moderate inverse correlation with the degree of smoking. The mean IgE level was 189.8 IU/ml in those who smoked 1-9 cigarettes/day but only 32.8 IU/ml in those who smoked 10-19 cigarettes per day and 11.1 IU/ml in those who smoked 20 or more cigarettes/day. The number of years a person smoked did not seem to significantly influence the IgE level. The mean IgE level in ex-smokers (50.5 IU/ml) was much lower than in current light smokers but was still higher than in nonsmokers. There was a moderate inverse correlation between IgE levels and duration of cessation of smoking. Our data suggest a characteristic pattern for the influence of cigarette smoking on serum IgE level, namely, a striking rise associated with light smoking and a remarkable drop in heavy smokers, and such changes seemed reversible after the habit was stopped. Smoking status, therefore, appears to be an important consideration in interpreting serum IgE levels and in revising the "norms" of IgE levels.

Interest in food allergy has increased among physicians as well as the public. The symptoms are mainly in the gastrointestinal tract, the skin, and the respiratory system. Other organs are less commonly affected. The offending food can be suspected from the medical history, by skin testing, or by serum-specific IgE antibodies (RAST). Verification, however, depends on documentation of disappearance of symptoms after avoidance of the offending food and their recurrence on reintroduction of that food. Treatment is mainly dietary avoidance. Its success, however, depends on many factors. Pharmacologic agents may be needed in some cases for symptomatic relief and possibly for prophylaxis. The awareness on the part of the primary physician of the manifestations of food allergy and its diagnosis should enhance the physician's expertise in dealing with such patients regarding further management.

The increasing awareness by the medical profession, as well as the public, of food allergy imposes the parallel task of accurate diagnosis and proper treatment. A carefully obtained medical history and a properly conducted elimination-challenge test are the most valuable as well as the least expensive procedures for diagnosis. Other selected in vivo and in vitro tests may enhance the diagnostic ability and may verify the immunologic basis of the food-induced reaction. Treatment is basically dietary avoidance, and its success depends on several factors. Pharmacologic agents may be needed for symptomatic treatment, and in certain instances for prophylaxis. The need still exists for developing an effective procedure of hyposensitization.

Sera of 17 patients with gluten-induced celiac disease were studied. Total serum IgE and IgD, as well as specific IgE and IgD antibodies to selected food antigens, were determined. Total IgE levels were within the normal range. Specific IgE antibodies to wheat, alpha-gliadin, cows's milk, rice and buckwheat were comparable to those of normal controls. In the celiac subjects total IgD levels were also within the normal range but IgD antibodies to wheat were high whereas IgD antibodies to milk were lower than in pooled normal sera. The levels of IgE or IgD antibodies to either wheat or milk showed no relationship to the presence of precipitins to the antigens of these two foods. The study did not demonstrate a role for IgE in celiac disease. That IgD antibodies may play a role is suggested by the elevated serum IgD antibodies to wheat antigens.